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Is prostacyclin responsible for producing the hyperdynamic response during early sepsis?
1Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence 02903, USA. pwang@lifespan.org
Critical Care Medicine
|June 2, 2000
Summary
Prostacyclin (PGI2) does not cause the hyperdynamic response in early sepsis. Inhibiting PGI2 synthesis did not prevent increased cardiovascular function, suggesting other mediators are responsible.
Area of Science:
- Sepsis Pathophysiology
- Cardiovascular Physiology
- Prostanoid Signaling
Background:
- Polymicrobial sepsis exhibits distinct hyperdynamic and hypodynamic phases.
- The role of prostacyclin (prostaglandin I2, PGI2) in early sepsis hyperdynamic state is unclear.
Purpose of the Study:
- To investigate if inhibiting PGI2 synthesis prevents the hyperdynamic response in early sepsis.
- To determine the contribution of PGI2 to early sepsis-induced cardiovascular changes.
Main Methods:
- Adult male Sprague-Dawley rats underwent cecal ligation and puncture (CLP) to induce sepsis.
- Plasma 6-keto-PGF1alpha (a PGI2 metabolite) levels were measured via radioimmunoassay.
- A PGI2 synthase inhibitor, tranylcypromine, was administered to assess its effect on cardiovascular parameters and PGI2 levels.
- Left ventricular pressure changes and microvascular blood flow were analyzed.
Main Results:
- Plasma 6-keto-PGF1alpha levels significantly increased post-CLP.
- Hyperdynamic cardiovascular responses, including increased cardiac output and microvascular blood flow, were observed.
- Inhibition of PGI2 synthesis did not attenuate these hyperdynamic responses.
Conclusions:
- PGI2 is not the primary mediator of the hyperdynamic cardiovascular response in early sepsis.
- Other signaling pathways likely drive the hyperdynamic state observed in early sepsis.